• Gary Nieman, Joshua Satalin, Penny Andrews, Kailyn Wilcox, Hani Aiash, Sarah Baker, Michaela Kollisch-Singule, Maria Madden, Louis Gatto, and Nader Habashi.
• SUNY Upstate Medical University, Syracuse, NY.
• J Trauma Acute Care Surg. 2018 Dec 1; 85 (6): 1081-1091.

AbstractThe acute respiratory distress syndrome (ARDS) remains a serious clinical problem with the current treatment being supportive in the form of mechanical ventilation. However, mechanical ventilation can be a double-edged sword; if set properly, it can significantly reduce ARDS associated mortality but if set improperly it can have unintended consequences causing a secondary ventilator induced lung injury (VILI). The hallmark of ARDS pathology is a heterogeneous lung injury, which predisposes the lung to a secondary VILI. The current standard of care approach is to wait until ARDS is well established and then apply a low tidal volume (LVt) strategy to avoid over-distending the remaining normal lung. However, even with the use of LVt strategy, the mortality of ARDS remains unacceptably high at ~40%. In this review, we analyze the lung pathophysiology associated with ARDS that renders the lung highly vulnerable to a secondary VILI. The current standard of care LVt strategy is critiqued as well as new strategies used in combination with LVt to protect the lung. Using the current understanding of alveolar mechanics (i.e. the dynamic change in alveolar size and shape with tidal ventilation) we provide a rationale for why the current protective ventilation strategies have not further reduced ARDS mortality. New strategies of protective ventilation based on dynamic physiology in the micro-environment (i.e. alveoli and alveolar ducts) are discussed. Current evidence suggests that alveolar inflation and deflation is viscoelastic in nature, with a fast and slow phase in both alveolar recruitment and collapse. Using this knowledge, a ventilation strategy with a prolonged time at inspiration would recruit alveoli and a brief release time at expiration would prevent alveolar collapse, converting heterogeneous to homogeneous lung inflation significantly reducing ARDS incidence and mortality.

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